The objective of these studies is to further explore the hypothesis that factors which reduce central respiratory drive in the young mammal may increase vulnerability to respiratory arrest following activation of the laryngeal reflex system. Our previous studies have shown that both iron deficiency anemia and growth retardation are associated with reduced respiratory drive, and that their effects are additive. It is not yet known whether this relates to reduced oxygen availability to the CNS, deficient neurotransmitter metabolism or abnormalities in peripheral adrenergic function. Important interrelationships among these factors are likely to occur. Studies will be carried out in piglets, 4 to 6 weeks of age. Those that develop spontaneous iron deficiency anemias, with or without growth retardation, will be compared with age-matched controls. Sensitivity to superior laryngeal nerve (SLN) stimulation will be explored in these, and compared with similar groups subjected to catecholamine depletion by giving reserpine 1-2 days prior to study. Respiratory drive will be assessed by measuring the maximal rate of change of airway pressure (dP/dt max), and by determining the duration of apnea which occurs during sustained supramaximal SLN stimulation. Catecholamine concentration in brain tissue will be determined in control, anemic and reserpinized piglets using the methods of Laverty and Taylor. The functional and biochemica changes assciated with repletion will be assessed following catecholamine infusions. The effects of cardiovascular alpha and beta activity will be studied by utilizing appropriate antagonists (phentolamine and practolol) and agonists (norepinephrine and isoproterenol) to determine their potential role in altering central respiratory drive. This should provide added evidence regarding changes in oxygen delivery to the CNS which may influence respiratory drive.